This proposal is concerned with adaptive bone remodeling of the femur following cementless and cemented total hip arthroplasty. Clinically, over 50% of the periprosthetic bone mass can be lost following hip arthroplasty. The practical health-related goal is to prolong implant survivorship and facilitate potential revision surgery by minimizing bone loss attributed to stress-shielding, the initial reduction in mechanical loading of the bone in the proximal femur due to load transfer through the prosthesis. The central hypothesis is that (in the absence of osteolysis related to degradation of the implant) stress-shielding represents the most important independent variable or "final common pathway" through which patient, implant and technical factors account for a large proportion of the bone loss following total hip arthroplasty. If this thesis is correct, then factors such as age and source of implant bonding (e.g., bone ingrowth versus cement fixation) play a role in the adaptive process, largely through mechanically-mediated pathways. The applicants propose to test their hypothesis by examining three of its implications: (i) individual variation in stress-shielding explains a large proportion of the individual variation in femoral bone loss following hip replacement; (ii) bone loss has the same relationship to stress-shielding in skeletally mature young and old animals following cementless hip replacement, even though the actual amount of bone loss may vary as a function of age; and (iii) bone loss has the same relationship to stress-shielding in cemented and cementless total hip arthroplasty. Individual estimates of stress-shielding will be made based on animal-specific finite element modeling of a canine model. These estimates will be correlated with measurements of change in periprosthetic bone mass made in the same animals. In this way, the actual variance in the dependent variable (change in bone mass), explained by variance in the independent variable (stress-shielding) and the nature of the relationship (linear or nonlinear), will be determined. Use of an animal model allows other causes of bone loss to be largely eliminated, thus permitting the effects of stress-shielding to be clearly defined.